Spontaneously hypertensive rats (SHR) develop hypertension, whereas their controls (Wistar-Kyoto rats: WKY) do not. Epinephrine (EPI) levels are elevated in brainstem areas implicated in controlling blood pressure in SHR during the development of hypertension, while Norepinephrine levels are depressed. After hypertension is firmly established and sympathetic nervous system activity decreases, central epinephrine levels drop and norepinephrine levels rise. The basic or general hypothesis underlying the proposed experiments is that epineprone and norepinephrine are modulators which determine the central nervous system "set" for blood pressure levels, and that derangement of the epinephrine/noreptinephrine ratio is a causative factor in the development of hypertension in SHR. PART A. Epinephrine neurons and their main groups of terminals in the brainstem of SHR and WKY will be localized and cmpared by immunocytochemistry using antibodies to the epinephrine biosynthetic enzyme phenylethanolamine-N-methyltransferase (PNMT). Norepinephrine containing cells will be destroyed by intraventricular administration of the neurotoxin 6-hydroxydopamine. Epinephrine containing neurons and their associated fluorescent varicosities will then be quantified to see if the number of cellular terminals, cell numbers, cell sizes, or cell location are increased in SHR as compared to WKY. The relationship between PNMT localization and epinephrine levels will be determined. PART B. Cyclic AMP is an intracellular mediator for many actions of epinephrine. The ability of epinephrine to aise cyclic AMP levels in brainstem slices will be determined. The nature of the adrenergic receptor responsible will be determined.